The antithrombotic profile of aspirin. Aspirin resistance, or simply failure?

Introduction Cyclooxygenase-1 [COX-1, prostaglandin synthase] catalyses the transformation of arachidonic acid to the unstable intermediate prostaglandin PGH2. Subsequently, thromboxane synthase acts on PGH2 to form TXA2, a transient biological product that induces platelet aggregation and is a powerful vasoconstrictor. Aspirin acts primarily by interfering with the biosynthesis of cyclic prostanoids: TXA2, prostacyclin, and other prostaglandins. It irreversibly inhibits COX-1 by acetylation of serine-530 and induces a long-lasting functional defect in the platelets. The resultant decrease in production of prostaglandins and TXA2 probably accounts for much of aspirin's antithrombotic effect [1,2]. The plasma half-life of aspirin is only 20 min in circulating blood. It is rapidly deacetylated and converted to salicylate in vivo. Salicylate does not affect COX-1 or COX-2 activity [3].